Modulation of Rapid Plasminogen Activator Inhibitor in Plasma by Stanozolol

1984 ◽  
Vol 51 (03) ◽  
pp. 396-397 ◽  
Author(s):  
J H Verheijen ◽  
D C Rijken ◽  
G T G Chang ◽  
F E Preston ◽  
C Kluft
Keyword(s):  
Oral Administration ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Fast Acting ◽  
Activator Inhibitor

SummaryFibrinolytic activity in plasma euglobulin fractions can be increased by oral administration of stanozolol. This increase is not caused by increased synthesis or release of tissue-type plasminogen activator. A decreased level of fast acting t-PA inhibition is very probably the cause of the higher activity. These results suggest that this inhibition has a regulatory role on fibrinolysis in vivo.

FIBRINOLYSIS AFTER HEART TRANSPLANTATION

1987 ◽  
Author(s):  
J A Páramo ◽  
R Arcas ◽  
J Fernández ◽  
J Herreros ◽  
R Llorens ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Cardiac Transplantation ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Inhibitor Activity ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Activator Inhibitor

Some aspects of the function of the fibrinolytic system were investigated in 12 patients undergoing cardiac transplantation. Plasminogen, euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor activity (PAI),α2-antiplasmin (α2-Ap) and fibrinogen degradation products (FDP) were determined preo-peratively and on postoperative days 1 and 5. Results showed a significant decrease of plasminogen (p <0.005), EFA (p <0.0001) and t-PA (p ^.0.001) on postoperative day 1 as compared to the baseline value, followed by recovery on day 5. There was a significant increase of PAI (p < 0 . 005) , α2-AP (p <0.0001) and FDP (p < 0.02) on postoperative day 1 as compared to the preoperative value. PAI and FDP reached the baseline value on postoperative day 5, but α2AP also increased on postoperative day 5. Our data show that there is an impairment in blood fibrinolytic activity early after cardiac transplantation, mainly related to a decrease of plasminogen and t-PA and a increase of PAI and α2AP. The clinical relevance of these data needs further evaluation.

Production of Tissue-Type Plasminogen Activator (t-PA) and Type-1 Plasminogen Activator Inhibitor (PAI-1) in Mildly Cirrhotic Rat Liver

1996 ◽  
Vol 75 (05) ◽  
pp. 801-807 ◽  
Author(s):  
Taiichiro Seki ◽  
Hideo Imai ◽  
Shigeyuki Uno ◽  
Toyohiko Ariga ◽  
Thomas D Gelehrter
Keyword(s):  
Plasminogen Activator ◽  
Rat Liver ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Activator Inhibitor ◽  
Pai 1

SummaryWe have studied the production of tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1) in liver of normal rats and in rats with mild cirrhosis induced by carbon tetrachloride inhalation, to demonstrate the production of these fibrinolytic components and their pathophysiologic role in the liver in vivo. Immunohistochemical study of paraffin-embedded liver sections and fibrin autography of frozen sections showed that the normal rat liver produces very little t-PA or PAI-1. On the contrary, striking t-PA activity and both t-PA and PAI-1 antigens were observed in the cirrhotic liver. Both t-PA and PAI-1 in plasma were also markedly increased in the cirrhotic rats. Because the hepatocyte can internalize t-PA or PA/PAI-1 complexes from circulation, Northern blot analysis of the total liver RNA was performed to demonstrate the endogenous synthesis of t-PA and PAI-1 in the liver. Although the normal liver hardly expresses either t-PA or PAI-1 mRNA, striking t-PA and PAI-1 mRNA expression was observed in the liver of rats with mild cirrhosis.These data demonstrate that t-PA and PAI-1 production is strongly upregulated in the liver in rats with mild cirrhosis. These fibrinolytic components, whose production is closely associated with liver failure, may play important roles in the regulation of hepatocyte proliferation and liver regeneration in vivo.

The Fast-Acting Inhibitor of Tissue-Type Plasminogen Activator in Plasma Is also the Primary Plasma Inhibitor of Urokinase

1986 ◽  
Vol 55 (01) ◽  
pp. 065-069 ◽  
Author(s):  
Egbert K.O Kruithof ◽  
Chiên Tran-Thang ◽  
Fedor Bachmann
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Order Rate Constant ◽  
Tissue Type ◽  
Subsequent Formation ◽  
Prolonged Incubation ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Fast Acting ◽  
Activator Inhibitor

SummaryWe have compared the ability of a plasminogen activator inhibitor (PA-inhibitor) in human plasma, to form complexes with radioiodinated tissue-type plasminogen activator (t-PA) and high molecular weight urokinase (HMr-UK). Addition of 125I-t-PA (final concentration 10 IU/ml) or of 125I-HMr-UK (2 IU/ml) to a plasma containing 33 U/ml of PA-inhibitor resulted in the rapid formation of a 110,000 Mr complex of 125I-t-PA or a 95,000 Mr complex of 125I-HMr-UK with PA-inhibitor. Upon prolonged incubation of the plasma with 125I-HMr-UK a secondary complex of a Mr of 88,000 was observed, which probably derives from limited degradation of the 95,000 complex. Preincubation of the plasma with unlabelled t-PA, HMr-UK or LMr-UK at higher concentrations prevented the subsequent formation of complexes between radiolabelled PAs and the PA-inhibitor. These results thus demonstrate that t-PA and UK form complexes with the same PA-inhibitor. The rate of complex formation of 125I-t-PA or of 125I-HMr-UK with the plasma PA-inhibitor was similar (second order rate constant of association with PA-inhibitor in the order of 107 M−1s−1).

Effects of Moderate Alcohol Consumption on Platelet Function, Tissue-Type Plasminogen Activator and Plasminogen Activator Inhibitor

1990 ◽  
Vol 63 (03) ◽  
pp. 345-348 ◽  
Author(s):  
J Veenastra ◽  
C Kluft ◽  
Th Ockhuizen ◽  
H v d Pol ◽  
M Wedel ◽  
...  
Keyword(s):  
Alcohol Consumption ◽  
Plasminogen Activator ◽  
Platelet Function ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Moderate Alcohol Consumption ◽  
Tissue Type Plasminogen Activator ◽  
Postprandial Phase ◽  
Type Plasminogen Activator ◽  
Activator Inhibitor

SummaryShort-term effects of moderate alcohol consumption on platelet function, tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were studied in two age groups of volunteers (20–30 and 45–55 years), each consisting of eight healthy males. The alcohol (30 g in red port and wine) was consumed during a standard dinner. Two blood samples were drawn: one in the postprandial phase, and one the next morning after fasting overnight. Alcohol consumption tended to increase platelet aggregation and production of hydroxy fatty acids, reduced plasma t-PA activity and increased PAI activity in the postprandial phase. After the overnight fast the effects on t-PA and PAI had disappeared whereas at that time alcohol consumption tended to decrease platelet function. The effects of alcohol on t-PA and PAI activity appeared mainly in the older age group, whereas the t-PA activity in this group was already much lower, irrespective of alcohol consumption.

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